# Population-Level Trends in Lifestyle Factors and Early-Onset Breast, Colorectal, and Uterine Cancers

## TL;DR

Cancer rates in young women, especially under 30, are rising in the U.S., and this trend is linked to increasing obesity.

## Contribution

This study identifies a strong population-level correlation between obesity and early-onset breast, colorectal, and uterine cancers in young women.

## Key findings

- Colorectal cancer incidence increased by 6.9% annually in women under 30 years old.
- Obesity showed the strongest population-level correlation with all three cancers, especially in class III obesity.
- Alcohol use had a moderate positive correlation with cancer risk, while smoking and physical activity showed no significant correlation.

## Abstract

Cancer diagnoses in women younger than 50 years old are rising in the United States, including breast, colorectal, and uterine cancers. At the same time, obesity has become more common in young adults. Understanding whether these trends are occurring together may help guide prevention and early detection strategies. In this study, we used national cancer registry data (2001–2018) and national health survey data from the same years to describe how cancer rates and lifestyle factors changed over time in women aged 20–49 years. We found that these cancers increased most sharply in women under 30 years of age, and obesity prevalence also rose over the same period. These findings highlight an important public health concern and support the need for future individual-level studies to clarify drives of early-onset cancer and inform targeted prevention efforts.

Objective: To evaluate population-level temporal relationships between modifiable lifestyle factors and rising breast, colorectal and uterine cancer incidence rates among females under 50 years old. Methods: This retrospective ecological study utilized data from the United States Cancer Statistics (USCS) for cancer incidence, the National Health and Nutrition Examination Survey (NHANES) for health-related behaviors, and the Behavioral Risk Factor Surveillance System (BRFSS) for physical activity. Modifiable lifestyle factors analyzed included obesity (BMI ≥ 30 kg/m2), smoking, alcohol use, fiber and saturated fat intake, caloric intake, and physical activity. Trends were assessed using average annual percent change (AAPC), and population-level correlations between cancer incidence and lifestyle factors were evaluated using Pearson correlation coefficients. Results: Between 2001 and 2018, 914,659 breast, 144,130 colorectal, and 124,399 uterine cancer cases were identified. The largest increases in cancer incidence occurred in age groups under 30 years old. Colorectal cancer increased by 6.9%, followed by uterine cancer at 4.8% and breast cancer at 1.7%, all p < 0.001. When examining this age group by race, colorectal cancer increased by 8.0% (p < 0.001) annually in White women aged 20–24 years, while uterine cancer rose 4.8% (p < 0.001) in Hispanic women in the 20–24 and 25–29 year age groups. Breast cancer also increased by 2.0% (p < 0.001) per year in White women 25–29 years old. Smoking rates decreased, and alcohol consumption and obesity rates increased. No significant correlation was found between cancer incidence and smoking, caloric intake, saturated fat, or physical activity. A moderate positive correlation was identified between alcohol use and cancer risk (r = 0.55–0.67, p < 0.05). Obesity prevalence showed strong population-level temporal correlation with cancer incidence for all three cancers with stratified analysis demonstrating the strongest correlations in patients with class III obesity. Conclusions: From 2001 to 2018, the incidence of breast, colorectal, and uterine cancers increased most sharply among women under 30 years of age. Over the same period, obesity prevalence in this population also increased. These population-level observations are hypothesis-generating and require confirmation in individual-level, prospective studies to determine whether and how obesity and other lifestyle factors influence early-onset cancer risk.